The present invention pertains to devices for treating a failing heart and related methods for placing the devices. In particular, the invention pertains to splinting devices placed on the heart to reduce the radius of curvature and/or alter the geometry or shape of the heart to thereby reduce wall stress in the heart and improve the heart""s pumping performance. The devices and methods of the present invention are directed toward endovascular techniques used to facilitate placement of the splinting devices on the heart.
Heart failure is a common outcome in the progression of many forms of heart disease. Heart failure may be considered as the condition in which an abnormality of cardiac function is responsible for the inability of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues, or can do so only at an abnormally elevated filling pressure. There are many specific disease processes that can lead to heart failure. Typically these processes result in dilatation of the left ventricular chamber. Etiologies that can lead to this form of failure include idiopathic, valvular, viral, and ischemic cardiomyopathies, including ventricular aneurysms.
The process of ventricular dilatation is generally the result of chronic volume overload or specific damage to the myocardium. In a normal heart that is exposed to long term increased cardiac output requirements, for example, that of an athlete, there is an adaptive process of slight ventricular dilation and muscle myocyte hypertrophy. In this way, the heart fully compensates for the increased cardiac output requirements. With damage to the myocardium or chronic volume overload, however, there are increased it requirements put on the contracting myocardium to such a level that this compensated state is never achieved and the heart continues to dilate.
One problem with a large dilated left ventricle is that there is a significant increase in wall tension and/or stress both during diastolic filling and during systolic contraction. In a normal heart, the adaptation of muscle hypertrophy (thickening) and ventricular dilatation maintain a fairly constant wall tension for systolic contraction. However, in a failing heart, the ongoing dilatation is greater than the hypertrophy and the result is a rising wall tension requirement for systolic contraction. This is felt to be an ongoing insult to the muscle myocyte resulting in further muscle damage. The increase in wall stress also occurs during diastolic filling. Additionally, because of the lack of cardiac output, a rise in ventricular filling pressure generally results from several physiologic mechanisms. Moreover, in diastole there is both a diameter increase and a pressure increase over normal, both contributing to higher wall stress levels. The increase in diastolic wall stress is felt to be the primary contributor to ongoing dilatation of the chamber.
Mitral regurgitation is a condition whereby blood leaks through the mitral valve due to an improper positioning of the valve structures that causes the valve not to close entirely. Geometric abnormalities resulting from a dilated left ventricle may cause or exacerbate improper functioning of the mitral valve, including mitral valve regurgitation, by altering the normal position and dimension of the valve, particularly the Valve annulus.
Prior treatments for heart failure associated with such dilatation fall into three general categories. The first being pharmacological, for example, diuretics and ACE inhibitors. The second being assist systems, for example, pumps. Finally, surgical treatments also have been experimented with.
With respect to pharmacological treatments, diuretics have been used to reduce the workload of the heart by reducing blood volume and preload. Diuretics typically reduce extra cellular fluid which builds in congestive heart failure patients increasing preload conditions. Nitrates, arteriolar vasodilators, angiotensin converting enzyme (ACE) inhibitors have been used to treat heart failure through the reduction of cardiac workload by reducing afterload. Inotropes function to increase cardiac output by increasing the force and speed of cardiac muscle contraction. These drug therapies offer some beneficial effects but do not stop the progression of the disease.
Assist devices include mechanical pumps. Mechanical pumps reduce the load on the heart by performing all or part of the pumping function normally done by the heart. Currently, mechanical pumps are used to sustain the patient while a donor heart for transplantation becomes available for the patient.
There are at least four surgical procedures for treatment of heart failure associated with dilatation: 1) heart transplantation; 2) dynamic cardiomyoplasty; and 3) the Batista partial left ventriculectomy, and 4) the Jatene and Dor procedures for ischemic cardiomyopathy. These procedures are set forth in slightly more detail in U.S. application Ser. No. 09/532,049, filed Mar. 21, 2000, entitled xe2x80x9cSplint Assembly for Improving Cardiac Function in Hearts, and Method for Implanting the Splint Assembly,xe2x80x9d the entire disclosure of which is hereby incorporated by reference herein. Hereinafter, this application will be referred to as xe2x80x9cthe ""049 application.xe2x80x9d
Due to the drawbacks and limitations of the previous devices and techniques for treating a failing heart, including such a heart having dilated, infarcted, and/or aneurysmal tissue, there exists a need for alternative methods and devices that are less invasive and pose less risk to the patient, both after and during placement, and are likely to possess more clinical utility.
Thus, a more recent procedure for treating the various forms of heart failure discussed above includes placing devices on the heart to reduce the radius of curvature of the heart and/or alter the cross-sectional shape of the heart to reduce wall stress. The devices are configured to reduce the tension in the heart wall, and thereby reverse, stop or slow the disease process of a failing heart as it reduces the energy consumption of the failing heart, decreases isovolumetric contraction, increases isotonic contraction (sarcomere shortening), which in turn increases stroke volume. The devices reduce wall tension by changing chamber geometry or shape and/or changing the radius of curvature or cross-section of a heart chamber. These changes may occur during the entire cardiac cycle or during only a portion of the cardiac cycle. The devices of the present invention which reduce heart wall stress in this way can be referred to generally as xe2x80x9csplints.xe2x80x9d These splints can be in the form of external devices, as described in U.S. application Ser. No. 09/157,486, filed Sep. 21, 1998, entitled xe2x80x9cExternal Stress Reduction Device and Method,xe2x80x9d the entire disclosure of which is incorporated by reference herein, or in the form of transventricular elongate tension members with heart-engaging assemblies, typically in the form of anchor pads, disposed on each end configured to engage substantially opposite portions of the chamber wall, embodiments of which are disclosed in the ""049 application incorporated above.
An aspect of the present invention pertains to splint devices, and related splinting methods, for endovascular implantation on the heart. The splints of the present invention may be implanted endovascularly through remote vascular access sites. The inventive techniques and devices thus are minimally invasive and less risky to patients.
The advantages and purpose of the invention will be set forth in part in the description which follows, and in part will be obvious from the description, or may be learned by practice of the invention. The advantages and purpose of the invention will be realized and attained by means of the elements and combinations particularly pointed out in the appended claims.
According to an aspect of the invention, a method for placing a splint assembly transverse a heart chamber comprises providing an elongate member having a first end and a second end and a deployable heart-engaging assembly connected to at least the first end. The method further includes advancing the elongate member through vasculature structure and into the heart chamber such that the first end of the elongate member extends through a first location of a wall surrounding the heart chamber and the second end extends through a second location of the heart chamber wall substantially opposite the first location. A deployable heart-engaging assembly is deployed such that it engages with a first exterior surface portion of the heart chamber wall adjacent the first location. The elongate member is secured with respect to the heart with a second heart-engaging assembly connected to the second end. The second heart-engaging assembly engages with a second exterior surface portion of the heart chamber wall adjacent the second location.
Another aspect of the invention includes a splint assembly for treating a heart, comprising an elongate member configured to extend transverse a chamber of the heart and at least one heart-engaging assembly formed at least partially from portions forming the elongate member. The heart-engaging assembly has a collapsed configuration adapted to travel through a heart wall and an expanded configuration adapted to engage the heart wall.
Yet another aspect of the invention includes a delivery tool for delivering a transventricular splint assembly to a chamber of the heart, comprising a tubular member having a distal end and a proximal end, the distal end having a curved configuration and the tube defining a lumen configured to carry at least a portion of the splint assembly. The delivery tool further includes at least one support mechanism disposed proximate the distal end of the tubular member, the support mechanism being configured to stabilize the tubular member with respect to a heart wall surrounding the chamber. The tubular member is configured to be advanced through vasculature structure and into the heart chamber.